My apologies, KB.
1. In vivo models demonstrate FTO overexpression causes AML cells to become resistant to antimetabolites. FTO inhibition or knockdown resensitizes resistant AML models to the antimetabolite it was previously resistant to. Since this mechanism is exactly what we see in humans, I presume FTO/m6A mechanism plays out in humans. The conserved nature of m6a mRNA modifications in Eukaryotes is another strong indicator that there is a high level of agreement between mice and humans. Of course, they aren't identical, but I take significant confidence from models.
There are many more in vivo examples I could use, but I'm not at my computer. Apologies.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10807068/
I'd say 2 and 3 are price sensitive.
My apologies, KB. 1. In vivo models demonstrate FTO...
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